Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You and Your Team.

Learn More →

Mitochondrial Therapy for Parkinson Disease

Mitochondrial Therapy for Parkinson Disease EDITORIAL HE PRECISE causes of Parkinson disease however, the greatest effect was in the highest dosage of (PD) are beginning to be defined and in- 1200 mg/d. clude specific genetic mutations causal of Their data are supportive of the view that mitochon- autosomal dominant (alpha-synuclein mu- drial dysfunction does play a role in the pathogenesis of T tations) and recessive (Parkin muta- sporadic PD and that further research using coenzyme tions) phenotypes and for sporadic PD, an interaction be- Q at higher dosages should be studied. It will be im- 1,2 tween genetic and environmental factors. An important portant to define whether the defects of mitochondrial emerging molecular defect is impaired function of the mi- complexes I and II/III are acquired genetic mutations and tochondrial electron transport chain, particularly inhi- whether they are due to environmental toxins or pri- bition of complexes I and II/III, leading to failure of aden- mary congenital mutations, inherited maternally, which osine triphosphate synthesis. Inhibition of complex I by cause a genetic predisposition for PD. Clearly, the data MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) of the Parkinson Study Group in this article are intrigu- 3,4 can cause human parkinsonism. Schapira and col- ing and provocative therapeutic findings and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Neurology American Medical Association

Mitochondrial Therapy for Parkinson Disease

Rosenberg, Roger N.
JAMA Neurology , Volume 59 (10) – Oct 1, 2002
Download PDF
1 page
Read Article

Mitochondrial Therapy for Parkinson Disease

Abstract

EDITORIAL HE PRECISE causes of Parkinson disease however, the greatest effect was in the highest dosage of (PD) are beginning to be defined and in- 1200 mg/d. clude specific genetic mutations causal of Their data are supportive of the view that mitochon- autosomal dominant (alpha-synuclein mu- drial dysfunction does play a role in the pathogenesis of T tations) and recessive (Parkin muta- sporadic PD and that further research using coenzyme tions) phenotypes and for sporadic PD, an...
Loading next page...
 
/lp/american-medical-association/mitochondrial-therapy-for-parkinson-disease-SYIcdJ2bjy
Publisher
American Medical Association
Copyright
Copyright 2002 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
ISSN
2168-6149
eISSN
2168-6157
DOI
10.1001/archneur.59.10.1523
Publisher site
See Article on Publisher Site

Abstract

EDITORIAL HE PRECISE causes of Parkinson disease however, the greatest effect was in the highest dosage of (PD) are beginning to be defined and in- 1200 mg/d. clude specific genetic mutations causal of Their data are supportive of the view that mitochon- autosomal dominant (alpha-synuclein mu- drial dysfunction does play a role in the pathogenesis of T tations) and recessive (Parkin muta- sporadic PD and that further research using coenzyme tions) phenotypes and for sporadic PD, an interaction be- Q at higher dosages should be studied. It will be im- 1,2 tween genetic and environmental factors. An important portant to define whether the defects of mitochondrial emerging molecular defect is impaired function of the mi- complexes I and II/III are acquired genetic mutations and tochondrial electron transport chain, particularly inhi- whether they are due to environmental toxins or pri- bition of complexes I and II/III, leading to failure of aden- mary congenital mutations, inherited maternally, which osine triphosphate synthesis. Inhibition of complex I by cause a genetic predisposition for PD. Clearly, the data MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) of the Parkinson Study Group in this article are intrigu- 3,4 can cause human parkinsonism. Schapira and col- ing and provocative therapeutic findings and

Journal

JAMA Neurology – American Medical Association

Published: Oct 1, 2002

References

  • Genetics of Parkinson's disease.
    Vaughan, JR; Davis, MB; Wood, NW
  • Pathogenesis of Parkinson's disease.
    Sherer, TB; Betarbet, R; Greenamyre, JT
  • Chronic parkinsonism in humans due to a produce of meperidine-analog synthesis.
    Langston, JW; Ballard, P; Tetrud, JW; Irwin, I
  • Mechanisms of MPTP toxicity.
    Prezedborski, S; Jackson-Lewis, V

You’re reading a free preview. Subscribe to read the entire article.

Try 2 weeks free now

DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

or browse the journals available

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$499/year

Save searches from
Google Scholar,
PubMed

Create folders to
organize your research

Export folders, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

Sign up
for free
Start 14 day
Free Trial